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首页> 外文期刊>Endocrinology >IL-6 up-regulates the expression of rat LH receptors during granulosa cell differentiation
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IL-6 up-regulates the expression of rat LH receptors during granulosa cell differentiation

机译：IL-6在颗粒细胞分化过程中上调大鼠LH受体的表达

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摘要

IL-6 is produced in granulosa cells under normal physiological conditions, including during ovulation. However, the roles of IL-6 in ovarian function, including regulation of LH receptor (LHR) expression in granulosa cells, have not been explored in detail. The aim of this study was to identify the mechanism underlying the effect of IL-6 on LHR expression in the granulosa cells of female Wistar rats. Our results indicated that IL-6 clearly enhanced the FSH-induced LHR mRNA expression in a dose-dependent manner and did not stimulate cAMP accumulation by itself. The membrane protein level of LHR, assessed by a binding assay, was increased by FSH and was further enhanced by association with IL-6. Results of the luciferase assay, using promoter constructs of LHR 281 bp upstream of the translational start site, revealed that IL-6 increased the promoter activity induced by FSH, but this effect was not observed with treatment by IL-6 alone. This ability of IL-6 to enhance FSH-induced LHR mRNA expression was blocked by the Janus tyrosine kinase (JAK) pathway inhibitor, but not by the ERK1/2 inhibitor. Thus, we speculated that this IL-6 activity might be mediated by the JAK/signal transducer and activator of transcription pathway. In addition, IL-6 augmented FSH-induced IL-6 receptor α mRNA expression and FSH elevated IL-6 production in granulosa cells, which indicates that IL-6 may positively regulate paracrine and autocrine actions in granulosa cells. These results suggest that IL-6 up-regulates FSH-induced LHR production by increasing mRNA transcription, and JAK/signal transducer and activator of transcription 3 signaling is required for up-regulation by IL-6 in granulosa cells.
机译：IL-6在正常生理条件下（包括排卵期）在颗粒细胞中产生。但是，尚未详细探讨IL-6在卵巢功能中的作用，包括调节颗粒细胞中LH受体（LHR）表达的调控。这项研究的目的是确定IL-6对雌性Wistar大鼠颗粒细胞LHR表达的影响的潜在机制。我们的结果表明，IL-6明显以剂量依赖的方式增强了FSH诱导的LHR mRNA的表达，并且自身并未刺激cAMP的积累。通过结合测定评估的LHR膜蛋白水平通过FSH升高，并通过与IL-6结合而进一步提高。使用翻译起始位点上游LHR 281 bp的启动子构建体进行的荧光素酶分析结果表明，IL-6增加了FSH诱导的启动子活性，但单独使用IL-6不能观察到这种作用。 IL-6增强FSH诱导的LHR mRNA表达的这种能力被Janus酪氨酸激酶（JAK）途径抑制剂阻断，但未被ERK1 / 2抑制剂阻断。因此，我们推测该IL-6活性可能是由JAK /信号转导子和转录途径激活子介导的。此外，IL-6增强了FSH诱导的IL-6受体αmRNA表达，FSH增强了颗粒细胞中IL-6的产生，这表明IL-6可能正调控颗粒细胞的旁分泌和自分泌作用。这些结果表明，IL-6通过增加mRNA转录来上调FSH诱导的LHR产生，而JAK /信号转导子和转录3信号激活剂是颗粒细胞中IL-6上调所必需的。

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